nerve entrapments of the lower leg, ankle and foot in...

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Nerve Entrapments of the Lower Leg, Ankle and Foot in Sport Paul McCrory, 1,2,3 Simon Bell 4 and Chris Bradshaw 2 1 Department of Neurology, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia 2 Department of Sports Medicine, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia 3 Centre for Sports Medicine Research and Education and Brain Research Institute, University of Melbourne, Parkville, Victoria, Australia 4 Department of Orthopaedics, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 372 1. Anatomical Features of Nerve Entrapment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . 373 1.1 General Approach to Neurogenic Leg Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373 1.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373 1.3 Key Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373 1.4 Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 1.5 Investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 2. Specific Nerve Entrapment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 2.1 Saphenous Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 2.1.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 2.1.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 2.1.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 2.1.4 Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 2.1.5 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 2.1.6 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 2.2 Common Peroneal Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 2.2.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 2.2.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 2.2.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 2.2.4 Investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380 2.2.5 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380 2.3 Sural Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 2.3.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 2.3.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 2.3.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 2.3.4 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382 2.3.5 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 2.4 Tibial Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 2.4.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 2.4.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 2.4.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385 REVIEW ARTICLE Sports Med 2002; 32 (6): 371-391 0112-1642/02/0006-0371/$25.00/0 © Adis International Limited. All rights reserved.

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Page 1: Nerve Entrapments of the Lower Leg, Ankle and Foot in Sporthms.health.uq.edu.au/sportsmedicine/hmst7004/Ankle... · Nerve Entrapments of the Lower Leg, Ankle and Foot in Sport Paul

Nerve Entrapments of the Lower Leg,Ankle and Foot in SportPaul McCrory,1,2,3 Simon Bell4 and Chris Bradshaw2

1 Department of Neurology, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia

2 Department of Sports Medicine, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia

3 Centre for Sports Medicine Research and Education and Brain Research Institute, University of Melbourne, Parkville, Victoria, Australia

4 Department of Orthopaedics, Olympic Park Sports Medicine Centre, Melbourne, Victoria, Australia

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3721. Anatomical Features of Nerve Entrapment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . 373

1.1 General Approach to Neurogenic Leg Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3731.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3731.3 Key Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3731.4 Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3751.5 Investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375

2. Specific Nerve Entrapment Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3752.1 Saphenous Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375

2.1.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3752.1.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3752.1.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3762.1.4 Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3762.1.5 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3762.1.6 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376

2.2 Common Peroneal Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3772.2.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3772.2.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3772.2.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3792.2.4 Investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3802.2.5 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380

2.3 Sural Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3812.3.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3812.3.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3812.3.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3812.3.4 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3822.3.5 Surgical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383

2.4 Tibial Nerve . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3832.4.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3832.4.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3832.4.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385

REVIEW ARTICLE Sports Med 2002; 32 (6): 371-3910112-1642/02/0006-0371/$25.00/0

© Adis International Limited. All rights reserved.

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2.4.4 Investigation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3852.4.5 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3852.4.6 Surgical Treatment of Tarsal Tunnel Syndrome . . . . . . . . . . . . . . . . . . . . . . . 386

2.5 Plantar Interdigital Nerves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3862.5.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386

3. Other Neurogenic Causes of Exercise-Related Lower Limb Symptoms . . . . . . . . . . . . . . . . 3873.1 Muscle Cramp Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388

4. Overlap of Clinical Syndromes Causing Exercise-Related Leg Pain . . . . . . . . . . . . . . . . . . 3885. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389

Abstract Exercise-related leg pain is a common and yet difficult management problemin sports medicine. There are many common causes of such symptoms includingstress fractures and muscle compartment syndromes. There are also a number ofless common but important conditions including popliteal artery entrapment andnerve entrapment syndromes. Even for an astute clinician, distinction betweenthe different medical causes may be difficult given that many of their presentingfeatures overlap. This review highlights the common clinical presentations andraises a regional approach to the diagnosis of the neurogenic symptoms. In part,this overlapping presentation of different pathological conditions may be due toa common aetiological basis of many of these conditions namely, fascial dysfunc-tion. The same fascial restriction that predisposes to muscle compartment syn-dromes may also envelop the neurovascular structures within the leg resultingin either ischaemic or neurogenic symptoms. For many athletes with chronicexercise-related leg pain, combinations of such problems often coexist suggestinga more widespread fascial pathology. In our clinical experience, we often labelsuch patients as ‘fasciopaths’; however, the precise pathophysiological basis ofthis fascial problem remains to be elucidated. This review discusses the variousnerve entrapment syndromes in the lower limb that may result in exercise-relatedleg pain in the sporting context. The anatomy, clinical presentation, investigation,medical management and surgical treatment are discussed at length for each ofthe syndromes. It is clear from clinical experience that the outcome of surgicalmanagement of such syndromes fares much better where a clear dermatomal paindistribution is present or where focal weakness and/or sensory symptoms appro-priate for the nerve are present. In many situations, however, nonspecific leg painor vague nonlocalising sensory symptoms are present and in such situations,alternative diagnoses must be considered and investigated appropriately. As men-tioned above, many different pathologies may coexist in the lower limb and maybe a source of confusion for the clinician or alternatively may be the reason forpoor treatment outcomes.

Exercise-related leg pain represents one of themost common presentations in sports medicine.This is usually caused by musculoskeletal overuseinjuries, but not uncommonly, a neurogenic causemay be suspected. Because of the complex anat-omy of the leg, few clinicians have a detailed un-

derstanding of all the potential neurological causesof such pain.[1-5] To complicate matters further,many of the clinical presentations overlap, in spiteof the fact that the underlying pathophysiologymay be related to separate vascular, compartmentor neurological dysfunction. In this review, the rel-

372 McCrory et al.

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evant neurological syndromes will be discussedalong with their surgical management.

There are a variety of neurological causes forpain in this region apart from focal peripheralnerve entrapments. These include radicular painarising from compression or irritation of the lumbo-sacral nerve roots, referred pain from innervatedstructures of the spine, polyneuropathies, myopa-thies and other forms of muscle disease as well asthe various chronic regional pain syndromes. Thesewill not be discussed further in this review.

1. Anatomical Features of NerveEntrapment Syndromes

A summary of the nerves and their motor andsensory distribution where it relates to the leg is setout in table I. It must be emphasised that manynerve entrapment syndromes may present withnonspecific or poorly localised pain. Furthermore,the cutaneous dermatomal distribution is extreme-ly variable between individuals (figure 1).

1.1 General Approach to Neurogenic Leg Pain

Unless nerve entrapment syndromes produce‘hard’ neurological signs of motor weakness, sen-sory loss or change in tendon reflexes, specific di-agnosis may be difficult and often circumstantial.For this reason, a regional approach to the likelynerve entrapments may be useful and then the ap-

propriate electrophysiological studies sought if thediagnostic suspicion is sufficient.[1]

1.2 History

The aim of the history in a patient with possibleneurogenic leg pain is to determine the locationand timing of the pain, its mechanism of onset,degree of irritability, aggravating and relievingfactors, presence of other joint pain or swelling,previous local trauma and the presence of neuro-logical signs or symptoms. The previous history ofback pain and its response to treatment may beparticularly important in diagnosis. An occupa-tional and sporting history is similarly importantin determining the aetiology of such syndromes.[6]

1.3 Key Symptoms

There are a number of important symptoms thatshould be specifically sought for as they may indi-cate the presence of potentially serious neurologi-cal disease unrelated to the focal nerve entrap-ments being discussed in this review. For example,spinal cord disease may be suggested by sphincterdysfunction, spinal root or radicular disease by thepresence of focal weakness or dermatomal sensorydisturbance, vascular obstruction by claudicant legpain and occult malignancy by systemic symp-toms. Night pain or rest pain is a particularly im-portant symptom to assess since it may indicateinflammatory, malignant or infective causes ofpain. Patients reporting such symptoms should be

Table I. Nerves of the lower leg

Nerve Main branches in leg Motor innervation in leg Sensory distribution in leg

Femoral nerve Saphenous nerve, infra-patellarnerve

Nil Medial and anterior knee(infra-patellar branch) and medialleg, ankle and arch of foot(saphenous branch)

Common peroneal nerve Superficial peroneal nerve, deepperoneal nerve, lateralcutaneous nerve of calf, suralcommunicating nerve

Peroneus longus and brevis,tibialis anterior, extensor hallucislongus, extensor digitorum longus,peroneus tertius, extensordigitorum brevis

Lateral calf, dorsum of foot, 1stweb-space

Tibial nerve Anterior tibial nerve, posteriortibial nerve, sural nerve

Gastrocnemius, soleus, tibialisposterior, flexor digitorum longus,flexor hallucis longus

Lateral aspect of ankle and foot(sural nerve)

Exercise-Related Leg Pain 373

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immediately referred for neurological assessment.These include:

• Bladder or bowel dysfunction• Focal or global weakness in the lower limbs

Iliohypogastricnerve

(anterior andlateral cutaneous

branches)

Ilio-inguinalnerve

Obturatornerve

Intermediate andmedical cutaneous

nerve of thigh

Lateral cutaneousnerve of thigh

Genitofemoralnerve

Superior,medial

andinferiorclunealnerves

Saphenousnerve Lateral cutaneous

nerve of calf

Posteriorcutaneous

nerve of thigh

Superficialperoneal nerve

Sural nerve

Deep peronealnerve

Lateralplantarnerve

Medialplantarnerve

Calcanealbranches

of sural andtibial nerves

Saphenousnerve

Obturatornerve

Fig. 1. Cutaneous innervation in the lower limb.

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• Loss of sensation or ‘pins and needles’• Loss of coordination in the lower limbs• Systemic symptoms (e.g. fever, night sweats

and loss of bodyweight)• Night pain or rest pain• Lower limb or buttock pain that gets worse with

exercise• Unilateral leg pain and swelling.

1.4 Examination

Details of neurological examination skills arebeyond the scope of this article. Readers are re-ferred to general neurological texts for furtherreading.[7]

1.5 Investigations

In the management of most cases of leg painwhere a neurological diagnosis is suspected, spe-cific confirmatory tests such as nerve conductionstudies or electromyography should be sought.[8,9]

The main role of radiological imaging modalitiessuch as isotope bone scanning, ultrasound andmagnetic resonance imaging (MRI) relate to thedetection of bone and soft tissue lesions rather thanneurological disease.[10,11]

2. Specific Nerve Entrapment Syndromes

The various specific nerve entrapment syndromesare discussed separately. The list of references foreach syndrome is not meant to be exhaustive andreaders are referred to the general texts in the ref-erence list for further information.[9,12]

2.1 Saphenous Nerve

2.1.1 AnatomyThis is the longest sensory branch of the femo-

ral nerve arising from the L1,2,3 nerve roots. Thenerve leaves the femoral triangle to enter the ad-ductor canal (or subsartorial canal of Hunter) to-gether with the femoral artery and vein. The wallsof the canal comprise vastus medialis and adductorlongus muscle and the roof is bridged by the vasto-adductor membrane. The sartorius muscle covers

the proximal portion of the canal and also coversthe two terminal branches of the saphenous nerve,the infrapatellar branch and the descendingbranch[9,12] (figures 2 and 3).

The infra-patellar branch supplies the sensationto the medial portion of the joint and the overlyinganteromedial skin. The descending branch accom-panies the saphenous vein to supply the skin of themedial leg and foot (figure 2).

2.1.2 AetiologyThe nerve may be injured in the adductor canal

by local trauma, surgery or inflammatory condi-tions such as thrombophlebitis. In the region of theknee, surgery is the principal cause where thenerve may be injured or irritated at the site of an

ASIS

Pubictubercle

Femoralartery

and vein

Descending genicular

artery

Vastusmedialis

Infrapatellarbranch of

saphenous nerve

Femoralnerve

Saphenousnerve

Fig. 2. Anatomy of the femoral nerve and its distal branches.ASIS = anterior superior iliac spine.

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arthroscopic portal. Local injuries may similarlyresult in saphenous nerve symptoms either from

direct trauma or pes anserine bursitis, which mayirritate the nerve. Some authors have speculatedthat stretching the nerve during knee flexion maybe a biomechanical explanation of the aetiology ofthis condition especially where cases of saphenousnerve entrapment in bodybuilding have been re-ported.[13-17]

2.1.3 Clinical PresentationThe typical presentation is of claudicant or

exercise-related medial leg or knee pain. This con-dition may be easily confused with vascular dis-orders such as popliteal artery entrapment. Com-pression or percussion (Tinel’s sign) of the nervein the region of the adductor canal or where thenerve crosses the medial femoral condyle usuallyproduces pain or ‘tingling’ radiating to the medialmalleolus and occasionally more distally on themedial leg. Alteration of sensation in the cutaneousdistribution of the nerve may be present.[18] In ourexperience, entrapment or injury to the infrapatel-lar branch produces a poorly localised anteromed-ial knee pain. Apart from iatrogenic injury at thetime of arthroscopic knee surgery, this syndromeis most commonly seen in cyclists and rowerswhere the presumed mechanism relates to repeti-tive knee flexion.

2.1.4 InvestigationWhere diagnostic uncertainty exists, a local an-

aesthetic block of the nerve within the adductorcanal may help isolate the syndrome. Often post-exercise examination of the patient, with or with-out a local anaesthetic block, may be the crucialdiagnostic step.

2.1.5 ManagementTreatment may either be conservative or in-

volve surgical neurolysis.[19,20] Conservative treat-ment includes physiotherapy, ‘neuromeningeal’stretching and soft tissue massage.

2.1.6 Surgical ManagementSurgical treatment of saphenous nerve entrap-

ment, in general, involves exposure of the saphe-nous nerve in the subsartorial canal. The incisionis approximately 10cm proximal to the patella, an-

Femoralnerve

Obturatornerve

Lateralcutaneous

nerve of thigh

Lateralcutaneous

nerve of calf SaphenousnerveSuperficial

peroneal nerve

Sural nerve

Deepperoneal nerve

Distalbranch

of saphenousnerve

Infrapatellarbranch of

saphenousnerve

Saphenousnerve

Fig. 3. Anatomy of the saphenous nerve.

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terior to the sartorius. The interval between quad-riceps and sartorius is developed. The next layerencountered is the fascia between the vastus medialisand the adductor magnus. This is incised to exposethe saphenous nerve.

There is then argument as to whether neurolysisof the nerve or neurectomy gives the best result.One of the more detailed reports on surgical man-agement of this condition reported 15 patients withcomplete relief of symptoms in 13 knees. At theend of the study it was concluded that neurectomygave a more predictable result than neurolysis.[17]

The main problem with division of the saphenousnerve is the distal anaesthesia, which some patientsfind quite annoying.

If neurolysis is carried out all fascial bandsaround the saphenous nerve must be divided in themore distal regions of the subsartorial canal (figure3). If neurectomy is performed then the nerve isdivided proximal to the fascia in the canal betweenthe vastus medialis and adductor magnus. The bestmanagement for the cut proximal nerve is to sutureinto an adjacent muscle belly so that any distalneuroma will be less likely to cause future prob-lems.

The nerve can also be compressed as it travelsbetween the sartorius and gracilis muscles neartheir insertion. The nerve can either be released ordivided in this region.

Probably the most frequently seen problem inthe sporting population is a neuroma of the in-frapatellar branch. This can be irritated by repeti-tive movement of the knee or by direct pressureproducing symptoms from the neuroma. Surgicaltreatment is simple. A straight incision is madeover the neuroma, which is then excised, dividingthe infrapatellar branch fairly proximally.

2.2 Common Peroneal Nerve

2.2.1 AnatomyThe common peroneal nerve (CPN) leaves the

sciatic nerve in the distal thigh and lies on the bi-ceps femoris muscle and tendon to the poplitealfossa. It then runs laterally in an exposed fibro-

osseous tunnel at the level of the fibular neck andpasses below the tendinous origin of peroneuslongus and enters the peroneal tunnel between thetwo heads of this muscle. Proximal to the fibularhead, the lateral sural cutaneous nerve branchesfrom the CPN and passes distally. As the nerve entersthe peroneal tunnel, the CPN divides into the deep,superficial and recurrent peroneal nerves. Thesenerves stretch over the periosteum of the fibularneck and are covered by the tendinous origin of theperoneus longus muscle at this point. Plantarflexion or ankle inversion tenses peroneus longusand compresses the nerve in the tunnel against thefibula neck (figures 4 and 5).

The superficial peroneal nerve (SPN) runs be-tween the fibula and the peroneus longus muscleand courses distally lying on the anterior intermuscu-lar septum. The SPN supplies both peroneal mus-cles. At the junction of the middle and distal thirdof the tibia, the nerve pierces the crural fascia andsplits into two cutaneous branches. This nerve maybe compressed by the crural fascia (the SPN syn-drome) or where the terminal branches cross theanterior aspect of the ankle joint sub-cutaneously.The terminal branches provide the sensation to theanterolateral leg, the dorsum of the foot and thedorsal skin of the great, second, third and medialfourth toes.

The deep peroneal nerve (DPN) pierces the an-terior intermuscular septum and travels with theanterior tibial blood vessels between the tibialisanterior and either the extensor digitorum longusproximally or extensor hallucis longus distally. Inthis fashion, these muscles receive their innerva-tion from the DPN. The nerve enters the foot underthe cruciform ligament and supplies the sensationto the skin between the great and first toes and amedial branch to the extensor digitorum brevismuscle.[21]

2.2.2 AetiologyInjury to the main trunk of the CPN in the region

of the peroneal (or fibular) tunnel frequently iscaused by an external compressive source such astight plaster casts, knee surgery, osteophytes, sy-

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novial cysts or ganglions, sitting in a prolongedcrossed leg position (figure 5). Functional anatom-ical changes such as repetitive exercise involvinginversion and pronation (e.g. runners, cyclists andmachine operators) stretch the CPN against the fib-ular and fibrous arch of the peroneal tunnel result-ing in the clinical syndrome. Many cases are idio-

pathic in origin.[13,22] Only few cases of CPN en-trapment have been reported in runners.[23-25] In-volvement of the CPN or its branches may also beseen in conjunction with compartment syndromes,the DPN with an anterior compartment syndromeand the SPN with a lateral compartment syn-drome.[26] Examination of the patient after exercise

Sciatic nerve

Peronealtunnel

Deep peronealnerve

Lateral cutaneousnerve of calf

Branch toPeroneus

brevis muscle

Commonperoneal

nerve

Branch toExtensor

digitorum longusmuscle

Branch totibialis anterior

muscle

Branch toExtensor hallucis

longus muscle

Superficialperoneal

nerveBranch toExtensordigitorum

brevismuscle

Suralnerve

Deepperoneal

nerve

Saphenousnerve

Lateral cutaneousnerve of calf

Peroneuslongusmuscle

Superficialperoneal

nerve

Fig. 4. Anatomy of the common peroneal nerve and its branches.

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and palpation of muscle compartments and assess-ment of vascular function is important in the diag-nostic workup of this problem.

2.2.3 Clinical Presentation

Common Peroneal Nerve (CPN) SyndromeIn all reported cases running or other exercise

resulted in leg pain and numbness. Examinationpost-exercise confirmed the presence of muscleweakness, paraesthesia and a positive Tinel’s sign

at the level of the fibular neck. All patients weretreated surgically after failure of conservativemanagement with a high (90%) success rate. Theusual clinical syndrome involves pain in the regionof the nerve compression that subsequently spreadsto the sensory distribution of the nerve. This exercise-related pain often resembles that of an anteriorcompartment syndrome. In our experience, thesubjective numbness may be variable in distribu-tion and is typically described as a characteristic

Commonperoneal nerve

Peroneuslongusmuscle

Lateralcutaneous

nerve of calf

Common peronealnerve passing

throughperoneal (fibular)

tunnel

Lateralcollateralligament

Superficialbranch of

peroneal nerve

Deep (profundus)branch of peroneal nerve

Fig. 5. Anatomy of the peroneal (or fibular) tunnel.

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‘burning’ sensation rather than ‘pins and needles’or a ‘loss’ of sensation. Compression or percussionof the nerve in the peroneal tunnel will usually in-crease the patient’s pain but not their other sensorysymptoms. Patients will usually have post-exerciseweakness of ankle dorsiflexion and inversion. Forcedinversion may increase the pain. Florid motor weak-ness, such as foot drop, is typically seen only latein the syndrome.

Superficial Peroneal Nerve (SPN) SyndromeClinical signs of the SPN syndrome include

pain or anaesthesia over the lateral calf and/or dor-sum of the foot with resisted ankle dorsiflexion andeversion.[21,27,28] SPN entrapment has been re-ported in runners, soccer players, jockeys, tennisplayers, bodybuilders and dancers.[12] In thesecases, loss of sensation during exercise over thelateral distal calf or dorsum of the foot was noted.Relief by conservative measures was uncom-mon.[27,29]

Deep Peroneal Nerve (DPN) SyndromeAll reported sports-related cases of DPN entrap-

ment relate to anterior tarsal tunnel syndrome(TTS) with symptoms referable to the dorsum ofthe foot rather than the lower leg.[12]

2.2.4 InvestigationsThe diagnosis may be confirmed with electro-

myography and nerve conduction studies that willusually demonstrate a localised slowing of CPNconduction across the peroneal tunnel. Specificelectrophysiological techniques also exist for theSPN and DPN branches.[30,31] Treatment may be con-servative with modification of the precipitating ac-tivity or biomechanical correction, or if this is un-successful, surgical decompression. If an underlyingcompartment syndrome is diagnosed with appro-priate pre- and post-exercise compartment pressurestudies then surgical decompression is recommended.

2.2.5 Surgical Management

CPNIf the CPN is compressed around the fibula neck

there are two common conditions that require sur-gical treatment. The first is compression of the

nerve related to a ganglion cyst arising from the prox-imal tibio-fibula joint. In most cases, the ganglionreaches the nerve via the sensory branch, which in-nervates the joint.[32,33] Surgical treatment for thiscondition is with excision of the ganglion cyst,which is followed proximally to the tibio-fibularjoint where it is excised, together with an area cap-sule in the joint, to try and prevent recurrence. Fol-lowing this a neurolysis is carried out of the nervearound the neck of the fibula, which may requiremeticulous dissection. It has been suggested thatrestoration of nerve function is better if the surgeryis carried out early.[25,34]

The authors have found that the most commoncondition seen in our sports medicine practice iscompression neuropathy of the peroneal nervearound the fibular neck. This is related to pressurefrom the overlying muscle and fascia, particularlyin the area where the nerve travels under the sharpfibrous edge of the peroneus longus origin[23] (fig-ure 5). We have found good relief of symptomswith release of the nerve around the fibular neck.

Surgical procedure for CPN compression aroundthe fibular neck involves an oblique incision alongthe course of the nerve. The fascia over the pero-neal muscles is divided exposing the deeper mus-cle belly, which is divided, exposing the nerve, to-gether with the sharp fibrous edge at the proximalentry of the nerve into the peroneus longus. Therecovery from decompression of the CPN of thefibular neck region is usually quite rapid and pa-tients can be running within 2 to 3 weeks.

SPNOperative treatment involves release and de-

compression of the nerve. The exact procedure de-pends on the pathology present. If there is a chroniccompartment syndrome, which in our experienceis uncommonly associated with this condition, thena standard compartment decompression is carriedout. It is then important to identify the course ofthe superficial branch where it travels from the pe-roneal to the anterior compartment. The anatomyin this region is extremely variable and all sites ofpotential compression need to be released. An oc-

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casional finding is compression of the nerve by amuscle herniation through a fascial hiatus. Thiscan even produce localised narrowing of the nerve.The pathology, in this situation, is enlargement ofa normal vascular fascial hiatus, due to the under-lying compartment syndrome, in an area where thenerve courses over the hiatus. With exercise, par-ticularly when a compartment syndrome is present,the underlying muscle belly herniates through thefascial defect, compressing the nerve. In this situ-ation, it is important to divide the fascia throughthe defect, extending this at least 5cm proximallyand distally.

When a compartment syndrome is not associ-ated with SPN compression, the nerve is usuallycompressed where it exits through the deep fas-cia,[35] or more distally.[36] In this situation a moredistal incision is necessary than for a compartmentdecompression. A longitudinal incision is madeanterior to the fibula and just proximal to the lateralmalleolus. Through this the fascia over the nerveat the exiting tunnel can be divided, together withdivision of any fascia covering the branching nervein the region of the transverse extensor retinacu-lum (transverse crural ligament). Styf[27] reportedthat only 9 of the 19 in their series were completelysatisfied with the procedure and this would reflectour experience. It appears that there can be chronicirreversible damage to the nerve in this condition.A form of ‘tension neuropathy’ has also been pro-posed for this distal form of SPN entrapment andthis responds to surgical release.[37,38]

DPNMost cases with this condition seen in our clinic

have been related to compartment syndrome withgood relief following decompression of the ante-rior and peroneal compartments. Less commonlyseen, but well described is the anterior TTS.[31] Inthis condition, the nerve is compressed under theextensor retinaculum. Compression has also beendescribed under the extensor hallucis brevis, andover dorsal osteophytes of the talo-navicular joint.

The nerve in all these areas is very superficial.The surgical approach is therefore directly over the

site of compression with resection of the osteo-phyte and neurolysis.

2.3 Sural Nerve

2.3.1 AnatomyThe sural nerve usually originates from two

main branches, the medial cutaneous sural nervefrom the tibial nerve and the ramus communicansof the lateral cutaneous sural nerve of the commonperoneal nerve. However, in up to 20% of cases,based on cadaver studies, the origins and course ofthe sural nerve were variably absent.[22,39]

The sural nerve begins with its main componentfrom the tibial nerve in the popliteal fossa and thenruns distally between the two heads of gastrocne-mius beneath the crural fascia. Between the middleand distal thirds of the calf, the nerve pierces thefascia and runs distally near the small saphenousvein lateral to the Achilles tendon. It anastomoseswith the common peroneal branch at different lev-els. The sural nerve then passes behind the lateralmalleolus to supply the ankle joint, the posteriorcalf and the lateral side of the heel and foot (figure6).[12]

2.3.2 AetiologyAlthough not commonly reported as a cause of

exercise-related leg pain nevertheless, compres-sion of the nerve caused by mass lesions, scar tis-sue, ganglia, surgical trauma and thrombophlebitishave all been reported. Extrinsic compressionfrom tight ski boots and casts may similarly inducethis problem. The crural fascia may act as either acompression point or a fixation point for the nerveand athletic activities such as running or tracksports may stretch the nerve at this level. Similarly,repetitive ankle inversion injuries may lead to fi-brosis and nerve entrapment.[3,15,40-42]

2.3.3 Clinical PresentationClinically, patients usually report shooting pain

or dysaesthesias in the cutaneous distribution ofthe nerve although objective signs may not alwaysbe present. In our experience, this neurogenic painis often confused with that of pathology in thetendo calcaneus and many athletes present to

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sports physicians with ‘recurrent’ Achilles tendon-itis or ‘tears’. The use of nerve conduction studiesto assist in diagnosis has been reported.[43]

2.3.4 ManagementTreatment of this condition depends on the ac-

curate clinical, radiological or electrophysiologi-

Saphenousnerve

Lateralcutaneous

nerve of calf

Calcanealbranches

Suralnerve

Tibialnerve

Suralnerve

Commonperoneal

(lateral popliteal)nerve

Sciaticnerve

Gastrocnemiusmuscle

Superficialfascia

Fig. 6. Anatomy of the sural nerve.

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cal identification of the lesion site. Dependingupon the nature of the underlying pathology orbiomechanical cause either a conservative or sur-gical approach may be considered.

2.3.5 Surgical ManagementIn the areas of potential entrapment, the sural

nerve is quite superficial and therefore once theregion of entrapment has been delineated, the sur-gical procedure is relatively simple.[41] A longitu-dinal incision is made over the involved area andthe overlying tissues within the subcutaneous re-gion divided. In the area around the heads of thegastrocnemius this may involve a long proximaldissection between the two muscle bellies.

2.4 Tibial Nerve

2.4.1 AnatomyThe tibial nerve originates from the anterior di-

visions of L4-S3 via the medial trunk of the sciaticnerve. The sciatic nerve divides into the commonperoneal and tibial nerves at the level of the popli-teal fossa and the tibial nerve continues distallydeep to gastrocnemius. In the calf this nerve sup-plies the muscular innervation to gastrocnemius,soleus, tibialis posterior, flexor digitorum longusand flexor hallucis longus. Approximately 15cmabove the ankle, the nerve becomes superficialpassing medial to the Achilles tendon. The nervethen passes underneath the flexor or medial reti-naculum of the ankle joint that forms the ‘roof’ ofthe tarsal tunnel. At the level of the tarsal tunnelthe nerve divides into the medial and lateral plantarnerves as well as the medial calcaneal branch thatsupplies the sensation to the medial aspect of theheel (figure 7).[44,45]

The tarsal tunnel is bridged by the retinaculumand the medial border of the tunnel is the talus andcalcaneus. The tibial nerve and its distal branchespass in distinct fascial tunnels separate to the othercontents of the tarsal tunnel which include the pos-terior tibial vessels and the tendons of tibialis pos-terior, flexor digitorum longus and flexor hallucislongus.[46] Compression of neural structures isknown as the TTS (figure 8).

The medial plantar nerve reaches the sole of thefoot by passing under the origin of abductor hallucisand through a fibro-osseous space formed by theattachment of flexor hallucis brevis to the calcaneus.The lateral plantar nerve passes separately under theabductor hallucis and then passes between flexordigitorum brevis and quadratus plantae. The lateralplantar nerve gives off a mixed sensory-motorbranch that passes in close relation to the plantarfacial attachment to the calcaneum. This nerve ul-timately innervates the abductor digiti quinti mus-cle. Injury to or entrapment of this branch has beenreported as a cause of persistent heel pain.[47-53] Bothplantar nerves end by forming the interdigitalnerves, the medial plantar forming the branches tothe medial three-and-a-half toes and the lateralplantar supplying the lateral one-and-a-half toes.The plantar nerves give the muscular innervationto all of the intrinsic foot muscles.

2.4.2 AetiologyFrom a clinical standpoint, injury or entrap-

ments affecting the tibial nerve in the leg arerare.[54] In the popliteal fossa, Baker’s cysts, pop-liteal artery aneurysms and ganglia can compressthe nerve but no specific sport or exercise-relatedconditions have been reported.[55] By contrast, en-trapment of the distal branches, most notably theposterior tibial nerve as it passes through the tarsaltunnel are extremely common in sport.[56,57]

The branches of the tibial nerve may also beentrapped distal to the tarsal tunnel in a variety ofspecific clinical syndromes. Although the causesof such injuries are generally the same as for theTTS, anatomically the point of entrapment tendsto be separate. The medial plantar nerve may be-come entrapped where it passes under the fibrousarch of the abductor hallucis origin and through thefibro-osseous space formed by the attachment offlexor hallucis brevis to the calcaneus.[3,58-60] Theauthors have seen a number of cases of isolatedmedial plantar nerve entrapment in ballet dancersrequiring surgical neurolysis for definitive cure.Isolated injuries to the lateral plantar nerve havealso been reported in gymnasts.[61]

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The first sensory-motor branch of the lateralplantar nerve may be entrapped between the mus-cle layers or where it passes in close relation to theplantar facial attachment to the calcaneum. Injury

to or entrapment of this branch has been reportedas a cause of persistent heel pain, although no neu-rological abnormalities are evident and the nervecan not be electrophysiologically tested. Surgical

Medialplantarnerve

Medialplantarnerve

Lateralplantarnerve

Lateralplantarnerve

Mediancalcanean

nerve

Tibial nerve

Commonperoneal

nerve

Branch toGastrocnemius

Branch toSoleus

Branch toPlantaris

Branch toPopliteus

Branch toTibialis

posterior

Branch toGastrocnemius

Branch toFlexor

digitorumlongus

Branch toFlexor

hallucislongus

Fig. 7. Anatomy of the tibial nerve.

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decompression may be successful in the manage-ment of this condition.[3,62]

The medial calcaneal branch of the tibial nervemay be entrapped in a TTS depending on the levelof branching. An ankle joint ganglion within thetarsal tunnel has been reported as a cause of entrap-ment of this particular nerve.[63] In the authors’experience most cases of neuropathy affecting thisnerve are secondary to extrinsic compression orlocal trauma not involving a TTS.

2.4.3 Clinical PresentationDamage to the tibial nerve or its branches within

the tarsal tunnel cause a characteristic clinical syn-drome of pain and/or paraesthesia in the foot.[64]

In the majority of cases, the TTS is secondary toexternal pressure, mass lesion or local bony andligamentous trauma to the ankle. In the sportingsituation, local tenoperiostitis has been cited as apotential cause although the clinical descriptions

of this in athletes are generally poor with the morelikely cause being biomechanical compression dueto rear foot pronation in such cases. Foot and ankleposition has a marked influence on tarsal tunnelcompartment pressure.[65] In many cases, idio-pathic fibrosis or ligamentous thickening havebeen the operative findings in typical cases.[3,59,66-72]

2.4.4 InvestigationInvestigation strategies for a suspected TTS

should include nerve conduction studies and electro-myography.[73] Numerous articles have been pub-lished discussing electrophysiological techniquesin this regard.[9,74-77] In addition, MRI may be use-ful to delineate the tarsal tunnel more accurately orif a local lesion or tumour is suspected.[11,78-81]

2.4.5 ManagementTreatment of TTS in the first instance should be

directed at correction of biomechanical abnormal-

Tibialisposteriormuscle

Flexor digitorumlongus muscle

Flexor hallucislongus muscle

Flexorretinaculum

Medial plantarartery

and nerve

Medialcalceneal

nerve

Abductorhallucis muscle

Lateralmalleolus Medial

malleolus

Medial plantarartery and nerve

Medialcalceneal

nerve

Lateral plantarartery and nerve

Lateral plantarartery and nerve

Calcaneus

Talus

PL

PB

Fig. 8. Anatomy of the tarsal tunnel. AH = abductor hallucis; FDL = flexor digitorum longus; FHL = flexor hallucis longus; PB = peroneusbrevis; PL = peroneus longus; TP = tibialis posterior.

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ities using orthotic devices, and footwear modifi-cation may be required. The use of local cortico-steroid injections or anti-inflammatory treatmentmay be useful in reducing inflammation if present,which may in turn reduce swelling in the tarsaltunnel providing relief of symptomatic nerve com-pression. It is important to note, however, that nerveinjury may result from incorrect injection tech-nique and that because of the complex anatomy, anyinjection must be inserted in the correct anatomicalplane to be effective (figure 8). If conservative mo-dalities fail to resolve the problem and the symp-toms are severe or disabling, then consideration ofsurgical exploration is necessary.[82,83]

2.4.6 Surgical Treatment of Tarsal Tunnel SyndromeA longitudinal incision is made mid-way be-

tween the medial malleolus and the Achilles ten-don. The dissection is continued down to the sheathof the flexor digitorum longus. In the plane overthis tendon the dissection is then carried more pos-teriorly. The neurovascular bundle is then identi-fied. There are usually one or two small vesselscoursing anteriorly in this region that need divisionwith a bipolar diathermy. The proximal portion ofthe flexor retinaculum is identified and the entireretinaculum is then divided just posterior to theflexion digitorum longus, taking care not to injurethe underlying neurovascular structures. Neuroly-sis is then carried out of the tibial nerve, which canbe followed to its division into the medial and lat-eral plantar nerves.

In cases where it is felt that the entrapment isalso distal to the tarsal tunnel, then a similar pro-cedure is carried out. However, dissection is car-ried more distally. The fibrous arch of the abductorhallucis origin, and the fibro-osseous space formedby the attachment of the flexor hallucis brevis isdivided. If clinically indicated, either the medialcalcaneal branch of the tibial nerve or the lateralplantar nerve and its first sensory branch can befollowed distally and overlying compressive struc-tures divided, with appropriate neurolysis. The me-dial calcaneal branch in at least 20% of cases con-

sists of multiple nerve branches. In one study, mul-tiple branches were found in 60% of cases.[84] Toexpose the lateral plantar nerve, it is not infrequentlynecessary to take down a portion of the dorsal halfof the origin of abductor hallucis from the calca-neus, which is usually a dense fibrous band.

2.5 Plantar Interdigital Nerves

2.5.1 AnatomyThe interdigital nerves are formed from the ter-

minal branches of the medial and lateral plantarnerves and pass distally alongside the metatarsalbones and cross the deep transverse metatarsal lig-aments (figure 7). The two syndromes that arecommonly recognised affecting these nerves inboth athletes and nonathletes are neuromas of theplantar interdigital nerves (Morton’s neuroma) andthe medial plantar proper digital nerve (Joplin’sneuritis).

Morton’s NeuromaAetiologyMorton’s neuromas result from damage to an

interdigital nerve where it lies on the deep trans-verse metatarsal ligament between the heads of ad-jacent metatarsal bones. This damage results in afibrotic nodule forming at that site with varyingdemyelination of the involved nerve.[85] Althoughcolloquially described as a ‘neuroma’, in fact thepathology is more typical of peri-neural fibro-sis.[86]

Clinical PresentationClinically, the patient complains of forefoot

pain that radiates into the toes that may or may notbe accompanied by a persistent sensory distur-bance. The characteristic pain is described as a lan-cinating or shooting pain when the metatarsalheads are compressed. Standing or walking usuallyexacerbates symptoms, particularly when wearingtight shoes.

InvestigationMorton’s neuromas can be directly imaged by

ultrasound, computed tomography and MRI scan-ning and the nerve can be tested electrophysiolog-ically.[87-89]

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ManagementTreatment may be conservative especially if

the symptoms are mild.[90] Footwear modification,metatarsal padding and corticosteroid infiltrationhave all been reported with varying degrees of suc-cess. If conservative measures are unsuccessfuland/or the symptoms severe, then surgical excisionof the neuroma, often combined with internal neu-rolysis, is the usual treatment.[91-93]

Surgical Treatment of Morton’s NeuromaThis has been described utilising either a plan-

tar or a dorsal approach. Controversy exists as tothe best surgical approach to this problem.[94] Thedorsal approach avoids making a scar on the soleof the foot. The transverse metatarsal ligamentneeds to be divided, and there is danger of damageto the dorsal cutaneous nerves in the web space.

The authors have mainly utilised a plantar ap-proach. A longitudinal incision is made, whichmust be accurately placed in the inter-space be-tween the metatarsal heads. Only sharp dissectionwith a knife should be carried out to avoid damageto the underlying fatty tissue. At times a largebursa may be present which needs to be removed.The common digital nerve is identified and tracedto its bifurcation and it is in this region that the‘neuroma’ occurs. The branches of the nerve aredivided and the common digital nerve is then cutproximal to the metatarsal head. The wound isclosed with interrupted suture.

Joplin’s NeuritisAetiologyJoplin’s neuritis is caused by a neuropathic in-

jury to the medial plantar proper digital nerve, ei-ther where it crosses the first metatarso-phalangealjoint or on the medial aspect of the great toe. Thisis usually caused by chronic compression or irrita-tion from inadequate footwear.[95]

Clinical PresentationTypically the patient complains of pain and par-

aesthesia on the medial side of the great toe whenwalking. In the authors’ experience, the symptomsoften commence after wearing particularly tightshoes and then remain as a persistent area of

localised sensory disturbance. There may addi-tionally be a biomechanical forefoot abnormalitythat predisposes the individual to this problem.The diagnosis may be confirmed by nerve conduc-tion studies. Treatment may be conservative withfootwear modification or surgical excision of thenerve performed for disabling or persistentpain.[96-98]

Surgical Treatment of Joplin’s NeuritisJoplin’s neuritis involves entrapment of the

proper digital nerve adjacent to the medial sesa-moid. Operative treatment may involve surgicalneurolysis and transposition of the nerve awayfrom the sesamoid or shaving a portion of the ses-amoid to assist in decompressing the nerve. A lesscommon condition is entrapment of the lateralproper digital nerve. It lies beneath the transversemetatarsal ligament, which produces pressurewhich then flattens the nerve. If symptoms are se-vere, then surgical treatment involves division ofthe deep transverse ligament and neurolysis of thenerve.

3. Other Neurogenic Causes ofExercise-Related Lower Limb Symptoms

Apart from the focal nerve entrapment syn-dromes, patients with other neurological condi-tions may present with symptoms referable to thelower limb. These may include myopathies, poly-neuropathies, exercise-related cramps or leg weak-ness due to proximal nerve injury. Muscle painmay occur following unaccustomed or extreme ex-ercise and may be severe and delayed in onset inits presentation. Clinicians need to be alert to thedifferential diagnostic possibilities in this situationand the patient history is the most important aspectof the overall assessment.

A patient with an underlying myopathic orneurogenic condition may present with a variety ofsymptoms. A feeling of ‘weakness’, ‘fatigue’ or‘tiredness’ is not unusual. Subjective muscle painis uncommonly reported in adults although muscletenderness may be noted. Localised muscle wast-ing may be present particularly in the inherited

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muscle diseases. If there is florid muscle weaknessthen the patient may present for diagnosis; how-ever, more usually a concerned parent or coach usu-ally notices the weakness that may be more evidentfollowing exercise. These symptoms are often bi-lateral and usually develop slowly. Some possiblediagnoses are listed in table II.

3.1 Muscle Cramp Syndromes

Muscle cramps represent sudden, involuntaryand often painful shortening of muscle, and maybe attended by visible ‘knotting’ of the musclewhich may in turn lead to abnormal posturing ofthe affected joint. These are perhaps the most com-mon neuromuscular disorders to affect an athleteand occur universally. For the most part their originis benign. The common cause of muscle cramps ismuscle fatigue; however, other factors such as de-hydration, vascular insufficiency, electrolyte im-balance or unaccustomed muscle activity may beassociated. Rare pathological causes include motorneuron disorders, hypothyroidism, muscle enzymedisorders or specific movement disorders such asIsaac’s syndrome. Treatment is usually symptom-atic and prevention by stretching, graduated exer-cise programmes and ensuring adequate hydrationbefore exercise is all that is usually required.[99]

4. Overlap of Clinical Syndromes Causing Exercise-Related Leg Pain

There is considerable clinical overlap betweenvascular entrapment, compartment syndromes andfocal nerve entrapments in cases of exercise-relatedleg pain. In some situations (e.g. with compartmentsyndrome affecting the peroneal or deep posteriorcompartments), exercise will produce neurogenicsymptoms. Similarly, popliteal artery entrapmentmay produce neural ischaemia resulting in focalneurological symptoms.

The astute clinician must first be aware of thevarious causes of exercise-related leg pain andtheir overlap, second, examine the patients follow-ing provocative exercise whilst the typical symp-

toms are present and third, appropriately investi-gate suspected cases to establish a pathophysiolog-ical diagnosis before definitive management. Formost sports medicine clinicians, the common causesof exercise-related leg pain relate to tibial stressfractures and other muscular problems. In caseswhere the presentation is atypical or where the pa-tient describes prominent neurological symptomsor where the initial bone investigations are un-revealing then consideration of the conditions de-scribed in this review may be helpful.

In a number of nerve entrapment syndromes in-volving the lower leg, a coexistent compartmentsyndrome is often diagnosed by the use of com-partment pressure studies. It has been our practicein this situation to carry out compartment decom-pression in addition to neurolysis of the involvednerve. For example, where a SPN entrapment isnoted and a clinical history of compartment syn-drome is elicited despite equivocal pressure stud-ies, a dual procedure is performed. In this proce-dure, a longitudinal incision is made ~4cm long,just anterior to the lateral intramuscular septum in

Table II. Causes of neurogenic lower limb weakness and pain otherthan nerve entrapments

Myopathic Inflammatory myopathies – polymyositisor dermatomyositis

Endocrine, toxic or drug-inducedmyopathies

Muscle dystrophies – limb girdle,scapulo-peroneal

Myotonic dystrophy

Acid maltase deficiency

Benign congenital myopathies –nemaline, myotubular

Neuromuscularblocking disorders

Myasthenia gravis

Lambert-Eaton syndrome

Guillain-Barre syndrome

Chronic demyelinating polyneuropathy

Neurogenic Diabetic amyotrophy

Root or lumbar plexus lesion

Motor neuron disease

Spinal muscle atrophy

Other Atrophy of muscles caused by jointdisease

Upper motor neuron lesion

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the mid-anterior compartment region. The anteriorcompartment fascia is divided longitudinally anda window of fascia is removed.[100] The peronealcompartment fascia is then divided longitudinallyand transversely, with removal of the smaller areaof fascia and the lateral intramuscular septum isalso divided. The superficial branch of the pero-neal nerve is identified and released as describedabove.

An overlap of different aetiological causes forclinical nerve entrapment syndromes is commonlyseen in sports medicine. In general terms, surgicaldecompression for localised nerve compressionfares better where a clear anatomic distribution ofpain exists. Caution must be exercised for thosepatients with non-anatomical complaints of pain orwhere additional neurological diagnoses exist suchas peripheral neuropathy or fibromyalgia. Evenathletes with long standing complaints of pain cando well with surgery, if carefully selected.

5. Conclusion

Numerous pathologies in the lower limb maypresent with chronic exercise-related leg pain. Fo-cal nerve entrapment syndromes represent a smallbut important group of conditions presenting to thesports physician. A detailed understanding of theanatomical basis and clinical presentation of suchconditions is presented in this article in order toguide clinicians in their management of such prob-lems. Many of the clinical presentations overlapand many of the described conditions coexist. Weraise the possibility of a common pathophysiolog-ical basis of many of these presentations; namelyfascial dysfunction. At the present time, however,the biochemical or genetic basis for such ‘fascio-pathies’ is unclear and should be an important di-rection of research in the future. Definitive surgi-cal management of focal nerve entrapments shouldbe based upon an appropriate clinical presentationaccompanied by electrophysiological abnormali-ties if treatment failure is to be avoided.

Acknowledgements

The authors have no conflicts of interest.

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Correspondence and offprints: Dr Paul McCrory, OlympicPark Sports Medicine Centre, Swan Street, Melbourne, VIC3004, Australia.E-mail: [email protected]

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